Experimental autoimmune neuritis

Abstract

AbstractExperimental autoimmune (allergic) neuritis (EAN), which is induced in various animal strains by immunization with peripheral nerve constituents, has been recognized as an animal model of human immune‐mediated neuritis; that is, Guillain–Barré syndrome or chronic inflammatory demyelinating neuritis. At first, EAN was reported in rabbits, and soon thereafter, in mice and rats. Various antigens relating to the peripheral nervous system (PNS) have also been reported. Symptomatic characteristics of EAN are quite similar despite different strains/antigens; that is, acute, self‐limiting, monophasic flaccid paralysis. However, modification of the antigen or administration of immune suppressants to EAN animals are able to induce chronic, relapsing demyelinating neuropathy. The cellular response and humoral kinetics, such as cytokine/chemokine/cell adhesion molecules in PNS of EAN animals, have been extensively studied. In the early 1990s, the dichotomy of type 1 T helper cells and type 2 T helper cells cellular response, along with the cytokine/chemokine milieu in EAN were investigated robustly; thereafter, type 17 T helper cells and regulating T cells followed. This sequence is very similar to what had been observed in human multiple sclerosis and experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis and somewhat counterpart of EAN. However, the PNS and central nervous system have several differences in respect to their cellular components, thus, the immune response that appears in EAN has some unique aspects. Investigation of these differences, and the mechanism of recovery and regeneration of PNS might provide us with better therapeutic options for PNS diseases, especially inflammatory neuropathy.